The differential role of L-selectin and ICAM-1 in Th1-type and Th2-type contact hypersensitivity.

Published

Journal Article

Sensitization and challenge using DNFB induce contact hypersensitivity (CHS) with predominant type 1 helper (Th1) cell infiltration, whereas those using FITC generate CHS with Th2 cell infiltration. CHS results from inflammatory cell infiltration, a process that is highly regulated by the expression of multiple adhesion molecules. We attempted to determine the role of L-selectin and ICAM-1 in Th1- and Th2-type CHS induced by DNFB or FITC in mice lacking either L-selectin, ICAM-1, or both. Th1-type CHS induced by DNFB was inhibited by L-selectin and/or ICAM-1 deficiency, which was associated with reduced IFN-gamma expression. Similarly, Th2-type CHS induced by FITC was inhibited by L-selectin deficiency. However, Th2-type CHS was increased by ICAM-1 deficiency and accompanied by increased Th2 cytokine expression. Infiltration of in vitro-generated Th1 cells into the FITC-challenged skin decreased in ICAM-1-deficient mice, whereas in vitro-generated Th2 cell infiltration increased, suggesting that ICAM-1 mediates Th1 cell migration and that in the absence of ICAM-1, Th1 cell recruitment decreased, whereas relative Th2 cell migration increased. These results suggest that ICAM-1 mediates Th1 cell recruitment irrespective of DNFB or FITC and that L-selectin recruits Th1 cells in Th1-type CHS, whereas it recruits Th2 cells in Th2-type CHS.

Full Text

Duke Authors

Cited Authors

  • Ogawa, A; Yoshizaki, A; Yanaba, K; Ogawa, F; Hara, T; Muroi, E; Takenaka, M; Shimizu, K; Hasegawa, M; Fujimoto, M; Tedder, TF; Sato, S

Published Date

  • June 2010

Published In

Volume / Issue

  • 130 / 6

Start / End Page

  • 1558 - 1570

PubMed ID

  • 20182448

Pubmed Central ID

  • 20182448

Electronic International Standard Serial Number (EISSN)

  • 1523-1747

Digital Object Identifier (DOI)

  • 10.1038/jid.2010.25

Language

  • eng

Conference Location

  • United States